Nitrogen-doped graphene quantum dots (N-GQDs) are safe for environmental release.
The role of microRNAs (miRNAs) in regulating innate immune response to Candida albicans infection in Caenorhabditis elegans is still largely unclear. Using small RNA SOLiD deep sequencing technique, we profiled the miRNAs that were dysregulated by C. albicans infection. We identified 16 miRNAs that were up-regulated and 4 miRNAs that were down-regulated in nematodes infected with C. albicans. Bioinformatics analysis implied that these dysregulated miRNAs may be involved in the control of many important biological processes. Using available mutants, we observed that mir-251 and mir-252 loss-of-function mutants were resistant to C. albicans infection, whereas mir-360 mutants were hypersensitive to C. albicans infection. The expression pattern of antimicrobial genes suggested that mir-251, mir-252, and mir-360 played crucial roles in regulating the innate immune response to C. albicans infection. Fungal burden might be closely associated with altered lifespan and innate immune response in mir-251, mir-252, and mir-360 mutants. Moreover, mir-251 and mir-252 might function downstream of p38 mitogen activated protein kinase (MAPK) or IGF-1/insulin-like pathway to regulate the innate immune response to C. albicans infection. Our results provide an important molecular basis for further elucidating how miRNA-mRNA networks may control the innate immune response to C. albicans infection.
The underlying molecular mechanisms for multi-walled carbon nanotube (MWCNT)-induced toxicity on innate immunity are still largely unclear. Considering the potential of for the study of innate immune response of animals, we employed this assay system to investigate the effects of MWCNTs on innate immune response of animals and the underlying mechanisms. Pre-exposure to MWCNTs at concentrations more than 100 μg L enhanced the adverse effect of fungal infection in reducing lifespan. With regard to the underlying cellular mechanisms, we found that MWCNT pre-exposure enhanced colony formation of in the body of nematodes, and suppressed innate immune response of nematodes by decreasing expression levels of some antimicrobial genes. With regard to the underlying molecular mechanisms, we found that MWCNTs decreased expression levels of, , and genes encoding the p38 mitogen activated protein kinase (MAPK) signaling pathway, and inhibited translational expression of PMK-1::GFP in the intestine and phosphorylation of PMK-1. Epistasis assays showed that MWCNTs required the involvement of the p38 MAPK signaling pathway mediated by a NSY-1-SEK-1-PMK-1 cascade to enhance the toxicity of fungal infection, increase fungal colony formation, and suppress innate immune response. Thus, our results suggest that MWCNTs may possess immunoinhibitory effects by affecting the functions of the p38 MAPK signaling pathway. Our study also provides meaningful insights into the role of innate immune system of hosts against the toxicity of environmental toxicants.
Background: Vitamin A belongs to an array of retinoids, which have a pivotal part in the development of embryo and fetus and is important in themorphogenesis and cellular differentiation of developing liver. Vascular endothelial growth factor (VEGF) and its receptor the vascular endothelial growth factor receptor 2 (VEGFR2) are known to regulate the formation of vasculature and organogenesis of liver. For the contribution of better enlightenment of the modulating effects of vitamin A on the developing liver we investigated the effect of vitamin A on the histology and immunohistochemical expression of VEGFR2 in the liver from the fetuses. Methods: For this purpose, eighteen pregnant albino mice were divided into three groups having six mice each. Group A served as control and was given 1ml of olive oil whereas group B and C were experimental groups and were given 0.6mg/kg and 1.8mg/kg of vitamin A diluted in 1ml of olive oil. Doses were given at 7th, 8th and 9th gestational days (GD). All animals were sacrificed at 18th GD and the livers from the fetuses were collected to observe the histological parameters such as inflammation, hepatic vacuolar degeneration, central vein diameter and hemorrhage in central veins along with immunohistochemical expression of VEGFR 2. Results: Results showed that vitamin A affected the histology of liver. Inflammation, hepatic vacuolar degeneration (HVD) and the central vein hemorrhages were increased significantly (p<0.001), while diameter of the central vein decreased (p<0.001) in group C as compared to group A and B. The immunohistochemical expression of VEGFR2 decreased in sinusoids of group C (p<0.001) as compared to group A and B. Conclusion: Thus, the maximum tolerated dose of vitamin A given to group C tends to affect the microarchitecture of the developing liver and expression of VEGFR2. Keywords: Vitamin A, Vascular endothelial growth factor, VEGF, vascular endothelial growth factor receptor 2,
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